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Báo cáo y học: " The Estradiol-Dihydrotestosterone model of prostate cancer"

Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học quốc tế cung cấp cho các bạn kiến thức về ngành y đề tài: The Estradiol-Dihydrotestosterone model of prostate cancer | Theoretical Biology and Medical Modelling BioMed Central Research Open Access The Estradiol-Dihydrotestosterone model of prostate cancer A Edward Friedman Address Department of Mathematics University of Chicago 5734 S. University Avenue Chicago IL 60637 USA Email A Edward Friedman - ed@math.uchicago.edu Corresponding author Published 18 March 2005 Received 08 February 2005 Theoretical Biology and Medical Modelling 2005 2 10 doi 10.1186 1742-4682-2-10 Accepted 18 March 2005 This article is available from http www.tbiomed.cOm content 2 1 10 2005 Friedman licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License http creativecommons.org licenses by 2.0 which permits unrestricted use distribution and reproduction in any medium provided the original work is properly cited. Abstract Background The exact relationship between hormonal activity and prostate cancer PCa has not yet been clearly defined. One of the key hormones associated with PCa is testosterone T . However both in vitro and in vivo studies have shown that under some conditions T is capable of either promoting PCa growth or death. This article proposes a theory which resolves this apparent paradox. Model The Estradiol-Dihydrotestosterone E-D model introduced in this paper proposes that 17P-estradiol E2 is essential for initiating the growth of PCa cells through the formation of telomeres. It also proposes that T is responsible for increasing the expression of proteins which cause apoptosis or programmed cell death and that 5a-dihydrotestosterone DHT is essential for preventing this. In addition it is known that some T is converted to both E2 and DHT which means that depending on the conditions T is capable of either promoting the growth of or the killing of PCa. Background There are currently two models for prostate cancer PCa which are diametrically opposed to each other. One model 1 proposes that high levels of androgens are .